An ethyl acetate fraction derived from Houttuynia cordata extract inhibits the production of inflammatory markers by suppressing NF-кB and MAPK activation in lipopolysaccharide-stimulated RAW 264.7 macrophages

Chun, Jin Mi; Nho, Kyoung Jin; Kim, Hyo Seon; Lee, A Yeong; Moon, Byeong Cheol; Kim, Ho Kyoung

doi:10.1186/1472-6882-14-234

Cited by 36 publications

(26 citation statements)

References 34 publications

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“…Similar to water extracts, ethyl acetate fraction of HC was also shown to suppress nuclear translocation of NF-κB p65 subunit and attenuated the activation of MAPKs (p38 and JNK) in LPS primed RAW 264.7 cells. Furthermore, the extract showed to significantly reduce the NO, PGE2, TNF-α and IL-6 levels (Chun et al, 2014).…”

Section: Potential Role Of H Cordata Against Inflammationmentioning

confidence: 90%

Therapeutic potentials of Houttuynia cordata Thunb. against inflammation and oxidative stress: A review

Shingnaisui

Dey

Manna

et al. 2018

Journal of Ethnopharmacology

121

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Section: Potential Role Of H Cordata Against Inflammationmentioning

confidence: 90%

Therapeutic potentials of Houttuynia cordata Thunb. against inflammation and oxidative stress: A review

Shingnaisui

Dey

Manna

et al. 2018

Journal of Ethnopharmacology

121

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“…MAPK, an intracellular serine/threonine protein kinase, is an important signaling system for cell-mediated extracellular signals to intracellular responses, and plays a key role in cell proliferation, apoptosis, in ammation, immunity and angiogenesis [22]. Studies have found that inhibiting MAPK signaling pathway activation can reduce the occurrence of in ammatory response [23]. So, this research postulated that MAPK might play an important regulatory role in the occurrence and development of vasculitis in Kawasaki disease.…”

Section: Discussionmentioning

confidence: 93%

Utilizing Network Pharmacology to Explore the Possible Mechanism of CoptidisRhizoma in Kawasaki Disease

Fan

Guo

2020

Preprint

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Background: Kawasaki disease (KD) isan acute self-limiting systemic vasculitis.In this study, a randomized controlled trial regarding berberine (main component of CoptidisRhizoma) function in treating KD was carried out and possible pharmacological mechanisms of CoptidisRhizoma (CR) on Kawasaki disease therapy were investigated using an integrated network pharmacology approach.Results: The BBR group was able to reduce the values of CRP, NLR and PLR significantly. Also, the effect of BBR improved the resistance rate of intravenous injection of gamma globulin significantly. In total, 9 compounds and 369 relative drug targets were collected from TCMSP, SWISS, SEA and STITCH database and 624 KD target genes were collected in DisGeNET, DrugBank and GeneCards database. The network analysis revealed that 41 targets might be the therapeutic targets of CR on KD, among which ATK1, RELA, SRC, CASP3 and MTOR ranked in top 5. Gene ontology enrichment analysis revealed that the reaction to bacteria-derived molecules and to lipopolysaccharide and the apoptosis process were the key biological procedures for CR treating KD. The KEGG pathway enrichment analysis pointed out that the four signaling pathways closely related to CR treating KD including age-rage signaling pathway, fluid shear stress and atherosclerosis, TNF signaling pathway and Toll-like receptor signaling pathway in diabetic complications.Conclusion: We concluded that the introduction of routine treatment combined with BBR in treating KD has advantages than routine treatment and can be considered as a preferred approach in KD. Network pharmacology showed that CR exerted the effect of prevention KD by regulating multi-targets and multi-components.

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“…However, the present study demonstrated through western blot analysis and immunofluorescence staining that the translocation of NF-κB was attenuated by lovastatin in LPS-stimulated RAW264.7 cells. Previously, studies have shown that NF-κB participates in the expression of iNOS and TNF-α (33)(34)(35). IκBα binds to NF-κB and suppresses its translocation; when IκBα is phosphorylated and degraded by proteasomes, NF-κB is activated and translocates into the nucleus (36).…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammatory effect of lovastatin is mediated via the modulation of NF-κB and inhibition of HDAC1 and the PI3K/Akt/mTOR pathway in RAW264.7 macrophages

et al. 2017

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Lovastatin is a 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor that is clinically used for the prevention of cardiovascular diseases. Although it has been reported that lovastatin has anti-inflammatory properties in several studies, how lovastatin regulates the inflammation is still unclear. To evaluate the effect of lovastatin on nitric oxide production (NO) in RAW264.7 macrophages, NO production assay was performed. Also, cell viability was measured to confirm cytotoxicity. Level of tumor necrosis factor-α (TNF-α) transcription was measured by reverse transcription polymerase chain reaction (RT-PCR) from total RNA in RAW264.7 cells. Western blot analysis and immunofluorescence staining were used to investigate the regulation of lovastatin on the expression, phosphorylation, and nuclear translocation of cellular proteins. The results of the present study revealed that lovastatin reduced nitric oxide production via the reduction of inducible nitric oxide synthase (iNOS) expression in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophage cells. The mRNA level of TNF-α was reduced in presence of lovastatin. In addition, lovastatin downregulated histone deacetylase 1 (HDAC1), resulting in the accumulation of acetylated histone H3 and heat shock protein 70. Furthermore, the expression of phosphoinositide 3-kinase catalytic subunits α and β was reduced under lovastatin treatment, and the phosphorylation of Akt and mammalian target of rapamycin was consequently inhibited. Lovastatin also inhibited the phosphorylation of inhibitor of nuclear factor (NF)-κBα and the translocation of NF-κB into the nucleus. Therefore, the present study demonstrates that lovastatin inhibits the expression of pro-inflammatory mediators, including iNOS and TNF-α, through the suppression of HDAC1 expression, PI3K/Akt phosphorylation and NF-κB translocation in LPS-stimulated RAW264.7 macrophage cells.

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An ethyl acetate fraction derived from Houttuynia cordata extract inhibits the production of inflammatory markers by suppressing NF-кB and MAPK activation in lipopolysaccharide-stimulated RAW 264.7 macrophages

Cited by 36 publications

References 34 publications

Therapeutic potentials of Houttuynia cordata Thunb. against inflammation and oxidative stress: A review

Therapeutic potentials of Houttuynia cordata Thunb. against inflammation and oxidative stress: A review

Utilizing Network Pharmacology to Explore the Possible Mechanism of CoptidisRhizoma in Kawasaki Disease

Anti-inflammatory effect of lovastatin is mediated via the modulation of NF-κB and inhibition of HDAC1 and the PI3K/Akt/mTOR pathway in RAW264.7 macrophages

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